This proposal will examine some of the potential determinants of perinatal transmission of HIV. Recently it was shown that the susceptibility of CD4+ T cells to HIV infection is related to both the quantity of b chemokine (MIP-1a, MIP-1 b and RANTES) produced by their CD4+ T cells and to the expression of the b chemokine receptor 5 (CCR5). This receptor was recently identified as the co-receptor for monocytotropic (M-tropic) isolates of HIV, which are the viruses that are mainly transmitted heterosexually and perinatally. Individuals who have homozygous mutations of the CCR5 receptor are resistant to HIV infection with M-tropic isolates. We will examine whether there is a correlation between either CCR5 expression or chemokine production and perinatal HIV transmission. As these chemokines also mediate CD8+ T-cell-mediated HIV suppression, which we have identified as an important early protective immune response in HIV-infected infants, we will also measure CD8 viral suppressive activity (CD8-VSA) to try to assess whether it also plays a role in perinatal HIV transmission. The laboratory was used for oligonucleotide synthesis, and recombinant DNA techniques.